A new paper1 reports findings for the first time on the beneficial effects of CoQ10 on bone, in which it enhanced bone-forming osteoblast differentiation while inhibiting osteoclast (bone resorbing cells) differentiation. These findings, while discovered in in vitro cell culture experiments, could be of particular value to postmenopausal osteoporosis that develops as a result of estrogen deficiency if the effects prove to work similarly in vivo.

At a dose of 100 μM, CoQ10 decreased the number of osteoclasts in cell culture to approximately 87.3% of controls (didn’t receive CoQ10).

The CoQ10 was found to work by its effects on specific bone signaling pathways. For example, RANKL (receptor activator of nuclear factor kappa B ligand) is released by preosteoblasts, which activates its receptor RANK that is expressed on osteoclasts with the monocyte/macrophage colony-stimulating factor (M-CSF) for osteoclastogenesis. Osteoclasts are bone cells that demineralize bone, hence decrease bone mineral density. The inhibition of the RANKL-induced osteoclast differentiation is one of the mechanisms for CoQ10 increase of bone formation. Another natural product that is reported to suppress RANKL-induced osteoclast differentiation is alpha lipoic acid.1

CoQ10 increased osteoblast differentiation by enhancing alkaline phosphatase (ALP) activity. “CoQ10 enhanced not only early osteoblastic biomarkers like ALP and Col1, but also late osteoblastic biomarkers such as BSP and matrix minralization through transcription factors Runx2 and OSX. In this way, CoQ10 acts as an enhancer for all stages of osteoblast differentiation.”1

The researchers suggest that further study be done to determine what the optimal dose of CoQ10 for bone formation should be. In the meantime, CoQ10 is quite safe. Sandy, for example, takes 100 mg. CoQ10 a day.

The authors sum up the results of their study: “… CoQ10 may have great therapeutic implications in treating osteoporosis and other bone diseases.”